Integrin alpha-4 beta-7 and Integrin alpha-E beta-7 (Integrin α4β7 and Integrin αEβ7)

Integrin alpha-4 beta-7 (α4β7) and Integrin alpha-E beta-7 (αEβ7) are heterodimeric cell surface receptors that belong to the integrin superfamily; they share the beta-7 (ITGB7) subunit but pair with different alpha subunits (ITGA4 and ITGAE, respectively)[1][6]. Both receptors are primarily expressed on subsets of lymphocytes. Integrin α4β7 mediates the migration and homing of lymphocytes to gut-associated lymphoid tissue through its interaction with MAdCAM-1, playing a critical role in gut immune surveillance and inflammation[1][6][7]. Integrin αEβ7 (CD103) is predominantly expressed on a subset of T cells in mucosal tissues; its main ligand is E-cadherin, enabling T cell retention within epithelial compartments, which is important for local immune responses and implicated in mucosal inflammation[3][4]. Both integrins are therapeutic targets in inflammatory bowel disease, with monoclonal antibodies such as vedolizumab (α4β7-specific) and etrolizumab (β7-specific, thus affecting both α4β7 and αEβ7) used or investigated for these indications[4]. Their key biological roles encompass cell adhesion, lymphocyte trafficking, and immune regulation[1][3][4][6].

Other names

For Integrin α4β7: Alpha-4/beta-7 integrin, LPAM-1, Peyer patches-specific homing receptor, ITGA4/ITGB7For Integrin αEβ7: Alpha-E/beta-7 integrin, CD103, ITGAE/ITGB7

Blockade of lymphocyte trafficking (vedolizumab and etrolizumab inhibit integrin-ligand interactions, preventing lymphocyte adhesion to gut endothelium[4]). Inhibition of gut homing and/or retention of T cells in mucosal tissues.